BTT-105 ameliorates hepatic fibrosis in non-alcoholic fatty liver animal model
DC Field | Value | Language |
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dc.contributor.author | Kim, Hye Young | - |
dc.contributor.author | Ahn, Sang Bong | - |
dc.contributor.author | Hong, Jeong-Min | - |
dc.contributor.author | Oh, Ju Hee | - |
dc.contributor.author | Saeed, Waqar Khalid | - |
dc.contributor.author | Kim, Gyu Sik | - |
dc.contributor.author | Kim, Hyun | - |
dc.contributor.author | Kang, Jong Koo | - |
dc.contributor.author | Kang, Sukmo | - |
dc.contributor.author | Jun, Dae Won | - |
dc.date.accessioned | 2022-07-06T11:41:04Z | - |
dc.date.available | 2022-07-06T11:41:04Z | - |
dc.date.created | 2021-12-08 | - |
dc.date.issued | 2021-11 | - |
dc.identifier.issn | 0892-6638 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/140511 | - |
dc.description.abstract | BTT-105 (1-O-hexyl-2,3,5-trimethylhydroquinone), a hydroquinone derivative, is a potent anti-oxidant that was safe and tolerable in phase I clinical trial. This study examined the anti-fibrotic effect of BTT-105 in a mouse model of non-alcoholic fatty liver disease (NAFLD) along with the underlying mechanisms. In vivo, efficacy of BTT-105 evaluated from three kinds of NAFLD models (methionine/choline deficient diet (MCD), high fat diet (HF) and western diet (WD)). Metabolomics and transcriptomics profiling analysis in liver tissues were conducted. In vitro, anti-fibrotic effect of BTT-105 assessed in human hepatic stellated cells (HSCs) and primary mouse HSCs. BTT-105 improved NAFLD activity score in three kinds of NAFLD animal models (MCD, HF, and WD). BTT-105 also decreased levels of hepatic pro-collagen and collagen fibers deposition in liver tissue. Metabolome and transcriptome analysis revealed that BTT-105 decreased lipid metabolites and increased antioxidants in NAFLD mice. In HepG2 cells, BTT-105 enhanced Nrf2-ARE reporter activity in a dose-dependent manner and increased the levels of antioxidant gene expression. BTT-105 showed inhibition of HSCs activation and migration. Gene expression profiling and protein expression showed that BTT-105 increased Nrf2 activation as well as decreased PI3K-Akt pathway in activated HSCs. BTT-105 attenuated ameliorates steatohepatitis and hepatic fibrosis. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | WILEY | - |
dc.title | BTT-105 ameliorates hepatic fibrosis in non-alcoholic fatty liver animal model | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Jun, Dae Won | - |
dc.identifier.doi | 10.1096/fj.202002656RRR | - |
dc.identifier.scopusid | 2-s2.0-85118133915 | - |
dc.identifier.wosid | 000712009200008 | - |
dc.identifier.bibliographicCitation | FASEB JOURNAL, v.35, no.11, pp.1 - 19 | - |
dc.relation.isPartOf | FASEB JOURNAL | - |
dc.citation.title | FASEB JOURNAL | - |
dc.citation.volume | 35 | - |
dc.citation.number | 11 | - |
dc.citation.startPage | 1 | - |
dc.citation.endPage | 19 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.isOpenAccess | N | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Life Sciences & Biomedicine - Other Topics | - |
dc.relation.journalResearchArea | Cell Biology | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Biology | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.subject.keywordPlus | NRF2 | - |
dc.subject.keywordPlus | MECHANISMS | - |
dc.subject.keywordPlus | 1-O-HEXYL-2,3,5-TRIMETHYLHYDROQUINONE | - |
dc.subject.keywordPlus | PROGRESSION | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | HX-1171 | - |
dc.subject.keywordAuthor | BTT-105 | - |
dc.subject.keywordAuthor | fibrosis | - |
dc.subject.keywordAuthor | non-alcoholic fatty liver disease | - |
dc.subject.keywordAuthor | non-alcoholic steatohepatitis | - |
dc.subject.keywordAuthor | Nrf2 | - |
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